The present invention relates to devices and methods for treating aneurysms. More particularly, the invention relates to devices and methods for treating abdominal aortic aneurysms including stents with self-expanding and balloon-expandable features.
An aneurysm is a sac formed by localized dilatation of the wall of an artery, a vein, or the heart. Common areas where aneurysms occur and cause potential medical conditions include the coronary arteries, the carotid arteries, various cerebral arteries, and the abdominal aorta. When a local dilatation of a vessel occurs, irregular blood flow patterns result, typically leading to accumulation of cellular material and thrombus formation. Typically, the wall of the vessel also progressively dilates and weakens, causing the aneurysmal sac to grow and often resulting in vessel rupture. Vessel rupture, in turn, often causes dramatic negative health consequences such as a stroke, when a cerebral vessel ruptures, or even death, when an abdominal aortic aneurysm (“AAA”) ruptures. In light of these consequences, improved treatment methods and devices for aneurysms are constantly being sought. Although the following discussion focuses on AAA treatment, it is equally applicable to aneurysms in other locations.
The abdominal aorta is the portion of the aorta (the body's largest artery) located within the abdominal cavity. It functions to carry blood from the heart to the lower extremities and abdominal organs. Typically, the abdominal aorta has a diameter of about 2 cm to 2.5 cm in an adult and extends in a relatively straight path from the heart towards the groin, bifurcating into the iliac arteries to supply blood to the legs.
Generally, AAA's are located within the aorta between the renal arteries superiorly and in the bifurcation into the iliac arteries inferiorly. Although at first an aneurysm may be quite small, as the disease process continues an aneurysm enlarges, the aorta wall thins, and rupture typically results. When the aneurysm is less than 4.5 cm in diameter, danger of rupture is quite low. Even before the aneurysm grows large enough to pose a danger of rupture, however, it may cause other problems. The enlarged region often develops a thrombus that fills the distension so that blood flows only down the central region. Pieces of clot may break off from the thrombus and be carried away, resulting in blockages in the legs, lungs or even the brain.
Furthermore, an aneurysm typically enlarges at a rate of 0.3-0.5 cm per year. An aneurysm of 8 cm in diameter has approximately a 75% per year rupture risk, with consequences of rupture often being fatal. About 15,000 people die each year in the United States from ruptured AAA's. Over 60% of people who suffer a ruptured AAA die before reaching a hospital. Those who survive long enough to undergo surgery typically face a 50% survival rate. Even if the aneurysm is discovered before rupture, surgical repair is difficult and risky although surgery is 95% successful.
Traditional AAA repair methods include open abdominal surgery, in which the AAA is accessed through the abdomen, the portion of the aorta containing the aneurysm is clamped off, the aorta is incised, clot is removed and the aorta is manually repaired with stents, graft material and/or other devices. Newer, endovascular repair techniques generally involve placing a device, including one or more stents and/or grafts across the aneurysm through the vasculature rather than via an open surgical procedure.
A stent is generally a hollow, cylindrical, expandable device used to prop open a blood vessel to preserve or restore it patency. Stents are usually made of metallic mesh-like material, which may be either self-expanding or manually expandable. Self-expanding stents have shape memory capabilities, so that they can be compressed into a smaller shape for positioning at an area of treatment and then allowed to expand to attach to the desired area. Expandable stents are typically positioned at a desired location and then expanded by an inflatable device, typically a balloon, to attach the stent in the desired location.
Another device commonly used in vascular repair is a vascular graft, typically made of a synthetic material such as polytetrafluoroethylene (PTFE). An advantage of these synthetic grafts is that they are extremely flexible and can be readily compressed to a very small size for endovascular insertion. Application of a graft alone, however, generally requires suturing of the graft to the wall of the aorta, which requires an open procedure.
Many currently available AAA devices combine one or more synthetic graft components with one or more stent components. The stent component generally anchors the device in a desired location and maintains the patency of the vessel, while the graft component prevents thrombus from entering through the mesh-like structure of the stent and reinforces the wall of the aorta. Typically, such a device is placed across a AAA, often through a large aortic thrombus, to act as a new blood vessel. For example, some devices include a stent component for placement above the aneurysm, near the renal arteries, a graft component to cross the aneurysm, and one or more additional stent components to anchor the device distal to the aneurysm.
One recurring problem in AAA repair with stent or stent-graft devices is stress placed on such devices by motion. One type of motion that effects a AAA repair device is bending motion by the patient. Currently available devices try to address such motion by either providing a stronger, stiffer stent-graft to minimize bending of the device or providing a more flexible device to minimize stresses on the device.
Another type of motion that stresses AAA stent-graft devices but which has been largely ignored in AAA stent-graft design is longitudinal movement, causing stretching and/or compression of a stent-graft. Such stretching and/or compression may occur in either of at least two ways—acute stretching or compression of the vasculature due to the patient's body motion and gradual stretching or compression of the vasculature as the aneurysm grows or shrinks due to the presence of the graft. This stretching or compression applies significant stresses to the proximal and distal seals of the graft, and can be one of the major causes of graft migration and leakage of the seals over time. It can also lead to structural failures of the stent-graft, such as separation of graft elements fracture in the body of the graft or the like.
Another frequent problem faced in AAA repair with stent-graft devices is leakage of blood around the outside of the device. Such leakage allows blood to circulate through the aneurysm, rather than through the device. This flow of blood outside the device causes the blood pressure within the aneurysm to increase and the size of the aneurysm to progressively grow, increasing the risk of rupture. One cause of such leakage is inadequate initial attachment of the device to the internal surface of the wall of the aorta proximal to the aneurysm. If attachment, or “anchoring” of the proximal portion of the device is inadequate, blood typically leaks between the device and the wall of the aorta, into the aneurysm.
Leakage of blood around a AAA stent-graft may also occur when such a device becomes loose after an initially adequate anchoring. In other words, even if a stent-graft is initially anchored sufficiently, the device may lose its tight fit after a period of use. A loosened stent-graft may slip distally, pushed by the flow of blood, which may further compromise the fit of the device within the aorta, causing further leakage. When such loosening, slippage and/or leakage occurs in currently available stent-graft devices, the devices must typically be replaced via an additional surgical procedure.
Generally, leakage around a AAA stent-graft is usually caused by one or more stresses on the device. Two types of stresses—bending and longitudinal—have been discussed above. A third type of stress on the seal of a AAA stent-graft is diametrical expansion and contraction of the blood vessel at the seal location over time, without matching expansion of the graft. This is caused both by cyclical variations in blood pressure, as well as gradual expansion or contraction of the blood vessel over time. A fourth stress is the hydrostatic pressure of blood against the graft. For the upper seal of the AAA graft system in the aorta, this pressure equals the cross-sectional area of the graft times the aortic blood pressure. For an aorta diameter of 26 mm, and a blood pressure cycling between 80 mmHg and 150 mmHg, this force equals 0.823 sq. in.*1.55 psi-2.90 psi, or 1.28-2.39 lbs. A similar estimate of the hydrostatic stress on an iliac seal of 14 mm diameter gives an estimate of 0.37-0.69 lbs.
When a graft such as a knitted Dacron graft is affixed to the inner surface of a human artery, the body's natural healing response causes ingrowth of endothelial tissue, scar tissue or pannus into the graft element. This healing response will typically create a hemostatic seal of the graft to the vessel wall over time, unless that healing response is disturbed by stresses or motion of the graft relative to the vessel wall. The tissue which forms this seal typically does not have significant structural strength, and the stent-graft may often be easily pulled loose or dissected from the vessel wall when due to one or more of the mechanical stresses described above.
Although efforts have been made to design a AAA stent-graft having a stronger graft-vessel wall connection, these attempts have met with limited success. Designing the graft to apply additional radial outward force against the vessel wall only gains a certain amount of longitudinal resistance to movement or migration. Building the graft with hooks or other anchors increases the risk of trauma to the vessel wall and the risk of fatigue failure of those anchoring elements. Evidently, strengthening fixation of the graft at the seal areas may be limited.
Therefore, it would be advantageous to have devices and methods to provide treatment of AAA with reduced leakage, slippage and breakage of the AAA stent-graft device. Ideally, devices would include adequate anchoring features to prevent both leakage and slippage of the device. There is also a need for a flexible device to allow for repeated bending, stretching and compression forces over time without breaking or significantly reducing the efficacy of the device. It would also be desirable for such devices to be adjustable once placed in a location in the aorta for treatment, so that devices which lose their fit within the aorta may be adjusted rather than replaced. At least some of these objectives will be met by the present invention.